Rejected

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used as analgesic and anti-inflammatory drugs. However, adverse effects, including gastrointestinal, renal, cardiovascular side effects, seriously complicate NSAIDs use. Their gastrointestinal side effects are the most known serious complications in patients taking these drugs. Previously we have shown that preconditioning stress attenuates the ulcerogenic action of indomethacin (IM) on the gastric mucosa. According our findings glucocorticoids, released in response to stressor, are gastroprotective hormones and involved in stress preconditioning protective effects. Corticotropin releasing factor (CRF), a major mediator of stress response, stimulates ACTH release through CRF receptors of subtype 1 and ACTH, in turn, stimulates glucocorticoid production. Here we verify the hypothesis that pharmacological preconditioning by CRF or ACTH can protect the gastric mucosa against ulcerogenic action of IM in rats through mechanism associated with glucocorticoids. For this, preliminary fasted (24 h) rats were administered by CRF (2.5 or 5 µg/ kg, ip) or ACTH (1U/kg, ip) 30 min before IM injection (35 mg/kg, sc). Gastric lesions were examined 4 h after IM administration. Plasma corticosterone levels were measured before and 4 h after IM injection. Since the gastrointestinal injury is accompanied by changes in somatic pain sensitivity, we also measured tail flick latencies (tail flick test) before and 4 h after IM. Both CRF and ACTH by itself caused an elevation of plasma corticosterone levels, which was accompanied by an increase of tail flick latencies (analgesic effect). IM administration resulted in the gastric erosion 4 h later. Pretreatment with CRF or ACTH reduced an area of gastric lesions caused by IM (gastroprotective effect). IM-induced gastric injury was accompanied by an increase of tail flick latencies, which was prevented by CRF (normalization of somatic pain sensitivity). To estimate the role of glucocorticoids in CRF-induced gastroprotection an inhibitor of corticosterone synthesis metyrapone (30 mg/kg) or CRF receptor type 1 antagonist NBI 27914 (10 mg/kg) or glucocorticoid receptor antagonist RU-38486 (20 mg/kg) was administered before CRF. Both metyrapone and NBI 27914 injected before CRF administration caused an inhibition of CRF-induced corticosterone response and prevented protective effect of CRF on the gastric mucosa against the IM-induced injury. The gastroprotective effect of CRF was also eliminated by the pretreatment with RU-38486. Thus, CRF as well as ACTH can protect the gastric mucosa against ulcerogenic action of IM. Gastroprotective action of CRF accompanied by normalization of somatic pain sensitivity is provided by mechanism associated with glucocorticoids.

Pain is a common and distressing symptom in people living with cancer that requires a patient-centred approach to management. Since 2010, the Australian Government has invested heavily in developing regional cancer centres to improve cancer outcomes. This study explored patient and carer experiences of care from a regional cancer centre with specific reference to cancer pain management.

Carbon monoxide accounts for thousands of deaths worldwide each year. Clinical effects can be diverse and include headache, dizziness, nausea, vomiting, syncope, seizures, coma, dysrhythmias, and cardiac ischemia, and severe toxicity generally affects the nervous and cardiovascular systems. Because of its complex pathophysiology, effects of toxicity can be acute or delayed. The diagnosis can be elusive, as carboxyhemoglobin levels do not always correlate with the degree of poisoning. Even when the diagnosis is certain, appropriate therapy is widely debated. Normobaric oxygen is the standard therapy, and the efficacy of hyperbaric oxygen is unclear.

Metallosis is a rare and poorly understood long-term complication of instrumented surgery that can result in an inflammatory pseudotumor termed metalloma. We describe a particularly unique case and compare it to 6 analogous cases identified by PubMed and/or Medline search through July 2020. A 79-year-old male with multiple prior spinal lumbar fusion procedures presented with progressive weakness and pain. Imaging revealed a large mass surrounding the right-sided paraspinal rod with extension into the spinal canal, neural foramina, extraforaminal spaces, psoas muscle, marrow spaces, and right sided pedicles. The case presented is a unique example of a unilateral metalloma with mixed-metal instrumentation that created a progressive neurologic deficit without infection, pseudoarthrosis, or hardware failure. This case highlights the lack of understanding regarding the pathophysiology of metallosis and metalloma in spinal instrumentation. We highlight the imaging findings of metalloma to encourage early identification for removal and decompression.

The precise mechanism of referred pain is not well understood; however, diaphragmatic irritation is a well-known etiology of referred pain. Left side referred pain due to diaphragmatic irritation is most commonly attributed to splenic laceration i.e. Kerr's sign. Here, we report an unusual case of left-sided referred pain that followed eating. An adult male presented vague and chronic left shoulder pain that followed eating. The pain was described as a deep boring type of discomfort that was poorly localized to the region deep to the acromion and extended superomedially along the upper fibers of the trapezius muscle. The pain was present immediately after eating heavy meals and always abated approximately 30 minutes later. There was no history of previous surgery and physical examination was unremarkable. CT examination of the abdomen and thorax did not show any pathology or anatomical variations that would result in such referred pain. Although the exact etiology of this case is unclear, the most likely cause would be left-sided diaphragmatic irritation from the stomach after eating. The current literature does not enclose reports pertaining to similar findings. Although unusual and seemingly rare, postprandial referred shoulder pain should be considered by clinicians alongside other causes of referred shoulder pain when presented with shoulder pain without an obvious musculoskeletal or neural etiology.

Urinothorax is a rare cause of pleural effusion, which is seen in patients with obstructive uropathy, blunt trauma, or ureteric injury during abdominal surgical procedures. Clinical symptoms may include dyspnea, chest pain, cough, fever, abdominal pain, and decreased urine output. Diagnosis is made by thoracentesis, which would reveal fluid with a urine-like odor, and pleural fluid analysis, which would show if fluid is transudative in nature with a pH lower than 7.30. Pleural fluid to serum creatine ratio of more than 1 is diagnostic for this condition. In our case, the patient underwent percutaneous nephrolithotripsy with a stent placement three days before presentation to the hospital. She was diagnosed with urinothorax, which led to further investigations, and she was found to have persistent hydronephrosis. Her condition improved after her underlying hydronephrosis was addressed with stent placement. She was discharged home in stable condition.

Background Dexmedetomidine, fentanyl, and tramadol as an adjuvant to local anesthetics improve postoperative analgesia when used in epidural anesthesia. We aimed to compare the efficacy of dexmedetomidine, fentanyl, and tramadol as an adjuvant to levobupivacaine in epidural anesthesia. Materials and methods This was a double-blinded randomized clinical trial (RCT). One-hundred twenty patients of either sex, aged 18-60 years, American Society of Anesthesiologists (ASA) physical status classification I and II, undergoing elective orthopedic procedures under epidural anesthesia were allocated into four groups of 30 each. The dexmedetomidine group received 15 ml of 0.5% levobupivacaine and 25 μg in 2 ml of dexmedetomidine, the fentanyl group received 15 ml of 0.5% levobupivacaine and 50 μg in 2 ml of fentanyl, the Tramadol group received 15 ml of 0.5% levobupivacaine and 100 mg of tramadol in 2 ml, and the control group received 15 ml of 0.5% levobupivacaine and 2 ml normal saline. Patients were monitored for the total duration of analgesia, time of first analgesic requirement, time to reach the T-10 level of sensory block, two-segment regression time of the sensory block, time to reach the motor block (Bromage 3), time to motor regression (Bromage 2), visual analog scale (VAS) scores at 0, 15 minutes, 30 minutes, and the first, second, sixth, twelfth, and twenty-fourth hours postoperatively, total analgesic consumption in 24 hours, and complications, if any, were recorded. Results During the inter-group comparison, VAS scores were lower, the duration of analgesia was longer, and the total analgesic consumption was less in the dexmedetomidine group compared to the fentanyl, tramadol, and control groups. The time to onset of sensory block to T-10 and the attainment of motor block up to Bromage 3 was lower in the dexmedetomidine group. Two segment regression and regression of motor block to Bromage score 2 was lowest for the dexmedetomidine group compared to the other groups. A lower incidence of hypotension and bradycardia was noted with dexmedetomidine. Conclusions Dexmedetomidine is the better alternative as an adjuvant to epidural anesthesia, with faster onset, good quality, and prolonged duration with no relevant adverse effects.

Pediatric intracranial aneurysms (PIA) are very rare and can be fatal if left untreated. There are many treatment strategies including microsurgical and endovascular techniques. We feel that endovascular treatment using trans-radial access (TRA) is safe and convenient for PIA compared to the trans-femoral access (TFA), which is commonly employed in this population. We present the case of the youngest patient in the world whose ruptured aneurysm was treated with endovascular coiling via the TRA. The seven-year-old patient was brought to the ER with a severe headache. He had several episodes of vomiting and an episode of seizure as well. Computerized tomography (CT) of the brain showed subarachnoid hemorrhage. A magnetic resonance angiogram (MRA) showed an aneurysm at the bifurcation of the right internal carotid artery (ICA). An intermediate catheter/microcatheter system was used to navigate up into the ICA and then into the aneurysm. Two coils were deployed with good packing. The patient had a good clinical recovery and is currently doing good without any neurological deficits. With the availability of newer devices, we believe the TRA will be widely used in the coming years. We need to have larger randomized controlled trials to really understand the advantages of TRA in this patient population.

Preeclampsia is characterized by hypertension and proteinuria, which is associated with kidney injury. Glycocalyx (GCX) degradation mediated endothelial injury can result in proteinuria and kidney damage. alpha 7 nicotinic acetylcholine receptor (α7nAChR) connects nervous and immune systems to respond to stress or injury. We aimed to explore the protective effect and mechanism of intraspinal analgesia on maternal kidney injury in preeclampsia. Endotoxin-induced preeclampsia rats treated with ropivacaine via intraspinal administration. Renal histopathological examination was performed, cell apoptosis in the kidney, the levels of Glycocalyx markers of Syndecan-1 and heparin sulfate (HS) in maternal serum, Syndecan-1 along with α7nAChR in the kidney were measured. Our results showed that kidney injury was obviously in preeclampsia rats with proteinuria, endothelial damage, higher apoptosis rate, increasing levels of Syndecan-1 and HS in serum, upregulated Syndecan-1 expression but downregulated α7nAChR expression in kidney. Preeclampsia rats treated with intraspinal injected ropivacaine attenuated preeclampsia-induced kidney injury as Syndecan-1 and HS were decreased in serum, Syndecan-1 expression was suppressed as well as α7nAChR was activated in the kidney. Our results suggested that Ropivacaine administered through the spinal canal may protect preeclampsia-induced renal injury by decreasing GCX and α7nAChR activation.